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PubMed1979

Effects of dependency among causes of death for cause elimination life table strategies.

A study is made of the effects of associated causes of death, and of dependency among causes of death, by observing the relative importance of one cause of death when another is eliminated under various competing risk models. Two disease pairs, cancer and infectious disease and stroke and ischemic heart disease, are selected for analysis because they represent different types of disease dependence. Crude probabilities of death for each disease are calculated for the U.S. white male population in 1969. Next, the effects of the complementary disease in a pair are hypothetically eliminated in one of three ways: (a) a standard competing risk adjustment for cause elimination when deaths are singly caused (Chiang, 1968), (b) lethal defect-pattern of failure computations for multiply caused death when no causal order is inferred (Manton et al., 1976), and (c) relative susceptibility, computations for multiply caused deaths when causes are ordered (Wong, 1977). The paper closes with a discussion of the relative merits of the three types of adjustments.

Actuarial Analysis↗
PubMed1989

Infant mortality by cause: a comparison of underlying and multiple cause designations.

The extent of variability in the social, economic, and demographic characteristics of infant deaths when grouped by detailed cause is analyzed using health statistics data for Florida for the period 1980-1982. "The analysis first compares cause-of-death-specific infant, neonatal, and postneonatal mortality between each of the four cause-of-death models. Next, interest shifts to an examination of the variability among decedents, specific to cause of death, in a range of background, proximate, and immediate determinants of infant health and survival. Variability is evident in cause-specific mortality rates as well as in decedent characteristics across the cause-of-death models. These findings suggest that more attention be given to the mode of identifying cause of death in studies of infant mortality." (SUMMARY IN FRE)

Americas↗
PubMed1998

Comparative evaluation of underlying causes of death processed by the Automated Classification of Medical Entities and the Underlying Cause of Death Selection Systems.

INTRODUCTION: The correct identification of the underlying cause of death and its precise assignment to a code from the International Classification of Diseases are important issues to achieve accurate and universally comparable mortality statistics. These factors, among other ones, led to the development of computer software programs in order to automatically identify the underlying cause of death. OBJECTIVE: This work was conceived to compare the underlying causes of death processed respectively by the Automated Classification of Medical Entities (ACME) and the "Sistema de Seleção de Causa Básica de Morte" (SCB) programs. MATERIAL AND METHOD: The comparative evaluation of the underlying causes of death processed respectively by ACME and SCB systems was performed using the input data file for the ACME system that included deaths which occurred in the State of S. Paulo from June to December 1993, totalling 129,104 records of the corresponding death certificates. The differences between underlying causes selected by ACME and SCB systems verified in the month of June, when considered as SCB errors, were used to correct and improve SCB processing logic and its decision tables. RESULTS: The processing of the underlying causes of death by the ACME and SCB systems resulted in 3,278 differences, that were analysed and ascribed to lack of answer to dialogue boxes during processing, to deaths due to human immunodeficiency virus [HIV] disease for which there was no specific provision in any of the systems, to coding and/or keying errors and to actual problems. The detailed analysis of these latter disclosed that the majority of the underlying causes of death processed by the SCB system were correct and that different interpretations were given to the mortality coding rules by each system, that some particular problems could not be explained with the available documentation and that a smaller proportion of problems were identified as SCB errors. CONCLUSION: These results, disclosing a very low and insignificant number of actual problems, guarantees the use of the version of the SCB system for the Ninth Revision of the International Classification of Diseases and assures the continuity of the work which is being undertaken for the Tenth Revision version.

Cause of Death↗
PubMed2024

Long-term exposure to particulate matter and all-cause and cause-specific mortality in an analysis of multiple Asian cohorts.

BACKGROUND: Exposure to ambient air pollution is associated with a significant number of deaths. Much of the evidence associating air pollution with adverse effects is from North American and Europe, partially due to incomplete data in other regions limiting location specific examinations. The aim of the current paper is to leverage satellite derived air quality data to examine the relationship between ambient particulate matter and all-cause and cause-specific mortality in Asia. METHODS: Six cohorts from the Asia Cohort Consortium provided residential information for participants, recruited between 1991 and 2008, across six countries (Bangladesh, India, Iran, Japan, South Korea, and Taiwan). Ambient particulate material (PM2·5) levels for the year of enrolment (or 1998 if enrolled earlier) were assigned utilizing satellite and sensor-based maps. Cox proportional models were used to examine the association between ambient air pollution and all-cause and cause-specific mortality (all cancer, lung cancer, cardiovascular and lung disease). Models were additionally adjusted for urbanicity (representing urban and built characteristics) and stratified by smoking status in secondary analyses. Country-specific findings were pooled via random-effects meta-analysis. FINDINGS: More than 300,000 participants across six cohorts were included, representing more than 4-million-person years. A positive relationship was observed between a 5 µg/m (Dockery et al., 1993) increase in PM2·5 and cardiovascular mortality (HR: 1·06, 95 % CI: 0.99, 1·13). The additional adjustment for urbanicity resulted in increased associations between PM2.5 and mortality outcomes, including all-cause mortality (1·04, 95 % CI: 0·97, 1·11). Results were generally similar regardless of whether one was a current, never, or ex-smoker. INTERPRETATION: Using satellite and remote sensing technology we showed that associations between PM2.5 and all-cause and cause-specific Hazard Ratios estimated are similar to those reported for U.S. and European cohorts. FUNDING: This project was supported by the Health Effects Institute. Grant number #4963-RFA/18-5. Specific funding support for individual cohorts is described in the Acknowledgements.

Humans↗
PubMed2006

Association between PM2.5 and all-cause and specific-cause mortality in 27 US communities.

While fine mode particulate matter (PM(2.5)) forms the basis for regulating particles in the US and other countries, there is a serious paucity of large population-based studies of its acute effect on mortality. To address this issue, we examined the association between PM(2.5) and both all-cause and specific-cause mortality using over 1.3 million deaths in 27 US communities between 1997 and 2002. A two-stage approach was used. First, the association between PM(2.5) and mortality in each community was quantified using a case-crossover design. Second, meta-analysis was used to estimate a summary effect over all 27 communities. Effect modification of age and gender was examined using interaction terms in the case-crossover model, while effect modification of community-specific characteristics including geographic location, annual PM(2.5) concentration above 15 microg/m(3) and central air conditioning prevalence was examined using meta-regression. We observed a 1.21% (95% CI 0.29, 2.14%) increase in all-cause mortality, a 1.78% (95% CI 0.20, 3.36%) increase in respiratory related mortality and a 1.03% (95% CI 0.02, 2.04%) increase in stroke related mortality with a 10 microg/m(3) increase in previous day's PM(2.5). The magnitude of these associations is more than triple that recently reported for PM(10), suggesting that combustion and traffic related particles are more toxic than larger sized particles. Effect modification occurred in all-cause and specific-cause deaths with greater effects in subjects >or=75 years of age. There was suggestive evidence that women may be more susceptible to PM(2.5) effects than men, and that effects were larger in the East than in the West. Increased prevalence of central air conditioning was associated with a decreased effect of PM(2.5). Our findings describe the magnitude of the effect on all-cause and specific-cause mortality, the modifiers of this association, and suggest that PM(2.5) may pose a public health risk even at or below current ambient levels.

Aged↗
PubMed2005

Plasma carotene and alpha-tocopherol in relation to 10-y all-cause and cause-specific mortality in European elderly: the Survey in Europe on Nutrition and the Elderly, a Concerted Action (SENECA).

BACKGROUND: Only a few observational studies have related plasma carotene and alpha-tocopherol to mortality in elderly subjects. OBJECTIVE: The objective was to study the association of plasma carotene (alpha-and beta-carotene) and alpha-tocopherol with all-cause and cause-specific mortality in elderly subjects who participated in a European prospective study. DESIGN: Plasma concentrations of carotene and alpha-tocopherol were measured in 1168 elderly men and women. After a follow-up period of 10 y, 388 persons had died. The association between plasma antioxidants and mortality was analyzed by using Cox proportional hazard models. To put our results in context, we performed a meta-analysis of 5 studies on plasma antioxidants and all-cause mortality in elderly populations. RESULTS: Plasma carotene concentrations were associated with a lower mortality risk [adjusted rate ratio (RR) for an increment of 0.39 micromol/L: 0.79; 95% CI: 0.70, 0.89]. This lower mortality risk was observed for both cancer (RR: 0.59; 95% CI: 0.44, 0.79) and cardiovascular disease (RR: 0.83; 95% CI: 0.70, 1.00). The lower risk of cardiovascular death was confined to those with a body mass index (in kg/m2) <25 (RR: 0.67; 95% CI: 0.49, 0.94). Plasma concentrations of alpha-tocopherol were not associated with all-cause or cause-specific mortality. The results for both plasma antioxidants and all-cause mortality were confirmed by the meta-analysis. CONCLUSIONS: This prospective study suggests that high plasma concentrations of carotene are associated both with lower mortality from all causes and with cancer in the elderly. For cardiovascular mortality, the inverse association was confined to elderly with body mass indexes <25.

Aged↗
PubMed1994

[Chagas' disease as main cause of death in the southeastern region of Brazil: presence of contributory causes].

Death certificates of all persons who died in in the State of S.Paulo, Brazil and which presented Chagas' disease as the principal cause of death, were studied with a view to analysing the existing additional information available as to contributory causes. After a direct reading of the 1,308 death certificates, the contributory causes were identified and registered. They were mentioned in 261 (20%) of the certificates, 185 of them presenting only one, and 75 two of them. The 6 more frequent contributory causes were: "megas", embolism, chronic pulmonary disease, infections (other than Chagas' disease), arterial hypertension and malnutrition. When analysing the presence of the contributory causes in two groups-persons of less than 50 years old, and those older than 50 a higher proportion of them was observed in the older group and a distinct profile of causes was found for each group. No statistic association was observed between contributory causes and sex or site of residence.

Adult↗
PubMed2006

[Probable cause of death after reclassification of ill-defined causes on hospital admissions forms in the Unified National Health System, Rio de Janeiro, Brazil].

This article describes the clinical and socio-demographic characteristics of deaths from ill-defined causes in the State of Rio de Janeiro, Brazil, in 1998, and reclassifies the groups of probable causes based on data from death certificates in the Mortality Information System and the Hospital Information System of the Unified National Health System (SIH-SUS) for 1997-98. Reclassification required a random sample of defined causes from the SIH-SUS. The technique used was probabilistic relationship of records. As compared to deaths with defined causes, in those with ill-defined causes the individuals were predominantly non-white, had less schooling, had died in Greater Metropolitan Rio de Janeiro, were less likely to have been hospitalized in the SUS, and were more likely to have died at home and without medical care. It was possible to reclassify 20% of deaths with ill-defined causes. Reclassification had a minor impact on proportional mortality, due to the size of this group (10% of the deaths). However, if the results could be applied to all deaths with ill-defined causes, the impact might be greater on proportional mortality.

Adolescent↗
PubMed1994

[Cause of death statistics (III). Sources for insurance medicine: cardiovascular diseases and selected causes of death].

Among cardiovascular diseases coronary artery disease ranks first as cause of death in the age group that is of importance for life insurance. It is the main cause of death in males age 30 and up. More females die from cerebral hemorrhage than from coronary artery disease. From age 50 upwards coronary artery disease is also the main cause of cardiovascular death in females. Over two thirds of all deaths due to gastrointestinal diseases are caused by liver disease, mainly cirrhosis of the liver. Chronic obstructive pulmonary disease causes two thirds of all respiratory deaths. Accidental deaths seem to be a male privilege, since only 20 per cent females are involved. Especially young males are at risk to get killed in an accident. The particular situation of accidents in the elderly mainly due to falls is discussed. Neurological, psychiatric illnesses, alcohol and drug addiction are discussed briefly. Males in general are more prone to commit suicide than females who account for only one quarter of all suicide deaths. Hanging was the preferred method. Young males especially are in danger of killing themselves. The importance of this new method of compiling vital statistics for life insurance purposes is discussed. These are the conclusions: 1. Main risk for life insurance is death due to cancer, mainly of the alimentary and respiratory tract. This applies to the population at large. In females breast and genital cancer are of crucial importance. 2. In males cardiovascular diseases cause slightly more deaths than tumors. From age 30 on coronary artery disease is the main cause of cardiovascular death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Delta opioid peptide [D-Ala2, D-Leu5]enkephalin causes a near complete blockade of the neuronal damage caused by a single high dose of methamphetamine: examining the role of p53.

The delta opioid peptide [D-Ala2, D-Leu5]enkephalin (DADLE) has been reported to block the neurotoxicity induced by multiple administrations of a moderate dose of methamphetamine (METH). We examined in this study if DADLE might block the neurotoxicity caused by a single high dose of METH in CD-1 mice. The levels of dopamine transporter (DAT), tyrosine hydroxylase (TH), major biogenic amines including DA, 5-hydroxytryptamine (5-HT), and their metabolites were examined. In addition, since the tumor suppressor p53 has been implicated in the neurotoxicity of METH, this study also examined the levels of p53 mRNA and protein affected by METH and DADLE. METH (25 mg/kg, i.p.) caused significant losses of DAT, TH, DA, 3,4-dihydroxyphenylacetic acid (DOPAC), and 5-HT in the striatum within 72 h. The administration of a single dose of DADLE (20 mg/kg, i.p., 30 min before METH) caused a complete blockade of all losses induced by METH except for that of the DA content (a approximately 50% blockade). DADLE did not affect the changes of rectal temperature induced by the administration of the high dose of METH. METH increased p53 mRNA in the striatum and the hippocampus of CD-1 mouse. DADLE abolished the p53 mRNA increase caused by METH. METH tended to increase the p53 protein level at earlier time points. However, METH significantly decreased the p53 protein level by about 30% at the 72-h time point. DADLE blocked both the increase of p53 mRNA and the decrease of p53 protein caused by METH. These results demonstrate a neuroprotective effect of DADLE against the neuronal damage and the alteration of p53 gene expression caused by a single high dose of METH. The results also indicate an apparent discordance between the protein level of p53 and the neurotoxicity caused by a high dose of METH. Synapse 39:305-312, 2001. Published 2001 Wiley-Liss, Inc.

Animals↗
PubMed2000

Cumulative cause-specific mortality for cancer patients in the presence of other causes: a crude analogue of relative survival.

A common population-based cancer progress measure for net survival (survival in the absence of other causes) of cancer patients is relative survival. Relative survival is defined as the ratio of a population of observed survivors in a cohort of cancer patients to the proportion of expected survivors in a comparable set of cancer-free individuals in the general public, thus giving a measure of excess mortality due to cancer. Relative survival was originally designed to address the question of whether or not there is evidence that patients have been cured. It has proven to be a useful survival measure in several areas, including the evaluation of cancer control efforts and the application of cure models. However, it is not representative of the actual survival patterns observed in a cohort of cancer patients. This paper suggests a measure for cumulative crude (in the presence of other causes) cause-specific probability of death for a population diagnosed with cancer. The measure does not use cause of death information which can be unreliable for population cancer registries. Point estimates and variances are derived for crude cause-specific probability of death using relative survival instead of cause of death information. Examples are given for men diagnosed with localized prostate cancer over the age of 70 and women diagnosed with regional breast cancer using Surveillance, Epidemiology and End Results (SEER) Program data. The examples emphasize the differences in crude and net mortality measures and suggest areas where a crude measure is more informative. Estimates of this type are especially important for older patients as new screening modalities detect cancers earlier and choice of treatment or even 'watchful waiting' become viable options. Published in 2000 by John Wiley & Sons, Ltd.

Aged↗
PubMed2003

Trends in mortality rates comparing underlying-cause and multiple-cause coding in an English population 1979-1998.

Until recently, national coding and analysis of routine mortality statistics in most countries included only underlying cause of death. There were changes in the rules for selection and coding of underlying cause in England in 1984 and 1993. We report on trends in mortality rates in an English region from 1979 to 1998, comparing multiple-cause and underlying-cause coded rates, for individual diseases that were affected by coding changes. Among many others, these include pneumonia, venous thromboembolism, heart failure, respiratory distress syndrome, tuberculosis, diabetes, dementia, alcohol and drug abuse, epilepsy, multiple sclerosis, stroke, asthma, peptic ulcer, appendicitis, and cancers of the breast, colon and prostate. Comparisons over time of mortality rates based on underlying cause alone will be misleading when the time-period crosses years in which rules changed for selecting underlying cause.

Cause of Death↗
PubMed2001

[Underlying cause of death from external causes: validation of official data in Recife, Pernambuco, Brazil].

OBJECTIVE: To validate the underlying cause of death recorded on the death certificates for individuals under 20 years of age who died from external causes in 1995 in Recife, Pernambuco, Brazil. METHODS: We divided the study into two stages, coding and validation. In both stages we compared the official data concerning causes of death to the data we obtained during our study. We grouped the death certificates into 5 broad categories according to the cause of death; we later subdivided them into 14 categories. We also individually compared the death certificates applying the four-digit system of the International Classification of Diseases, Ninth Revision (ICD-9). We assessed the agreement between the official data and our data in terms of sensitivity and the kappa coefficient. We took as the standard the categorization of the cause of death that we had made during our investigation. RESULTS: In the coding stage, considering all the external causes of death, the overall agreement between the official data and our study data was 94% for the 5 categories, 92% for the 14 categories, and 81% for the four-digit ICD-9 system. In the validation stage the overall agreement was 94% for the 5 categories, 91% for the 14 categories, and 73% for the four-digit ICD-9 system. CONCLUSIONS: Our results suggest that for the death certificates to be reliable, the Institute of Legal Medicine must fill them out following recommended standards. In addition, hospitals and police departments must use greater care in completing the transfer slips that accompany the bodies that are sent to the Institute. More accurate data need to be generated and disseminated for a society to better understand its patterns of violence.

Adolescent↗
PubMed2005

Leading causes of death in England and Wales--how should we group causes?

This article examines how best to identify the leading causes of mortality in England an Wales, by using different way of grouping causes of death, based on a list developed by the World Health Organization (WHO). Four different versions of this list are compared. The leading cause of death across all age groups depends on the ways in which common diseases and external causes are aggregated or disaggregated into groups. Areas of particular debate, examined in this article, are the grouping or splitting of accidents by mechanism and cancers by site within leading cause lists. These affect which causes appear in the top ten, and their order in different age groups.

Age Factors↗
PubMed1998

Improvement of the quality and comparability of causes-of-death statistics inside the European Community. EUROSTAT Task Force on "causes of death statistics".

BACKGROUND: Cause-of-death statistics are widely used for comparing health characteristics of European Community (EC) countries. Before attempting to interpret between-country differences, it is essential to assess the biases affecting the comparability of the data. EUROSTAT decided to address globally this problem with the objective to improve the quality and comparability of cause-of-death data within the EC. METHODS: The material is based on a review of results of international comparative cause-of-death studies and on specific inquiries among EC. Both cause-of-death certification and codification practices are analysed. Certification is studied comparing the models of death certificates, the type of information captured, certifiers training and querying practices. The different coding systems are analysed (International classification of diseases (ICD) in use, interpretation of the ICD rules, implementation of automated coding systems). RESULTS: International studies on comparability of certification and coding practices between countries are rare. These studies are based on certification of cases histories and recoding of samples of death certificates. Recent studies on respiratory diseases, cancers and diabetes outline differences that influenced on the reported level of mortality. The specific EUROSTAT investigation (1997) outline general discrepancies: models of death certificates, nature and amount of information entered, way to establish the diagnosis, degree of consistency of the certification process, autopsy practices, certifiers practices, implementation of ICD-10 and implementation of automated coding systems. CONCLUSION: EUROSTAT studies are now focused on causes of death requiring special attention for comparability (e.g. suicide, accidental deaths, drug and alcohol related deaths, unknown and ill-defined causes), on procedures to improve the homogeneity of certifiers training and querying practices, on the effect of the transition to ICD-10. The international model of death certificate recommended by the World Health Organization should be adopted as widely as possible. Uniform complementary information (e.g. surgery, pregnancy, autopsy, place of occurrence of accidental deaths, work accident) should also be adopted. The EUROSTAT investigations must result in definitions of common recommendations and guidelines to EC.

Cause of Death↗
PubMed2000

Glycogen synthase kinase-3 beta activity is critical for neuronal death caused by inhibiting phosphatidylinositol 3-kinase or Akt but not for death caused by nerve growth factor withdrawal.

Numerous studies reveal that phosphatidylinositol (PI) 3-kinase and Akt protein kinase are important mediators of cell survival. However, the survival-promoting mechanisms downstream of these enzymes remain uncharacterized. Glycogen synthase kinase-3 beta (GSK-3 beta), which is inhibited upon phosphorylation by Akt, was recently shown to function during cell death induced by PI 3-kinase inhibitors. In this study, we tested whether GSK-3 beta is critical for the death of sympathetic neurons caused by the withdrawal of their physiological survival factor, the nerve growth factor (NGF). Stimulation with NGF resulted in PI 3-kinase-dependent phosphorylation of GSK-3 beta and inhibition of its protein kinase activity, indicating that GSK-3 beta is targeted by PI 3-kinase/Akt in these neurons. Expression of the GSK-3 beta inhibitor Frat1, but not a mutant Frat1 protein that does not bind GSK-3 beta, rescued neurons from death caused by inhibiting PI 3-kinase. Similarly, expression of Frat1 or kinase-deficient GSK-3 beta reduced death caused by inhibiting Akt. In NGF-maintained neurons, overexpression of GSK-3 beta caused a small but significant decrease in survival. However, expression of neither Frat1, kinase-deficient GSK-3 beta, nor GSK-3-binding protein inhibited NGF withdrawal-induced death. Thus, although GSK-3 beta function is required for death caused by inactivation of PI 3-kinase and Akt, neuronal death caused by NGF withdrawal can proceed through GSK-3 beta-independent pathways.

Animals↗